General Neuro Questions For Final Flashcards

1
Q

Are the CR and the UCR different responses?

A

No. Same response to a different stimulus.

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2
Q

What is the Hebb rule?

A

Synapses active at the same time are strengthened over time

signs of this in rats: thicker cortex, more glial cells, more AChE

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3
Q

Describe the neural model of classical conditioning

A

The synapse is strengthened when an incoming action potential occurs at the same time as a postsynaptic action potential

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4
Q

Define reinforcement

A

A reinforcement makes a behavior more likely to occur in the future.

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5
Q

Define punishment.

A

A punishment makes a behavior less likely to occur in the future.

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6
Q

What is the “reward circuit”?

A

The Mesolimbic dopamine pathway. VTA->nucleus accumbens->amygdala->septum

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7
Q

Describe the mesocortical dopamine system.

A

VTA->PFC

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8
Q

What are the three phases of biological memory processes?

A
  1. Induction. Initiates modification processes
  2. Maintenance. The mechanisms that cause the modifications to stay
  3. Expression. How the modification is ultimately expressed.
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9
Q

What are the components of the hippocampus?

A

Dentate gyrus
Subicular complex
Hippocampus proper (CA regions)

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10
Q

Where does the entorhinal cortex receive input from?

A
  1. Amygdala
  2. Limbic cortex of the medial temporal lobe
  3. Association vortices (sensory, motor)

These may project directly, or via the perirhinal cortex, or parahippocampal cortex.

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11
Q

Where does the entorhinal cortex project to?

A

CA1, CA3, dentate gyrus

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12
Q

Where does the hippocampus output to?

A

Entorhinal, perirhinal, parahippocampal cortices

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13
Q

The primary output of the hippocampus comes from

A

The CA1 region and the subiculum

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14
Q

LTP requires:

A

Rapid stimulation of the perforant path

Activation of synapses and depolarization of the postsynaptic membrane

Activation of hippocampal NMDA receptors

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15
Q

Describe the process of LTP.

A
  1. Glutamate is released by presynaptic neuron
  2. AMPA receptor (not exotic) binds glutamate, allows Na+ to enter, depolarizers membrane
  3. NMDA (exotic) kicks off Mg2+ ion, Ca2+ enters cell
  4. Ca2+ entry triggers CAM-KII pathway cascade
  5. Phosphorylation of AMPA receptors (increased sensitivity/density)
  6. Production of NO synthase, arginine converted to NO
  7. NO diffuses into presynaptic cell, causes increase in glutamate release via cGMP, altered synaptic structure
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16
Q

LTP may result from:

A

Increased number of new AMPA receptors

Alternation of synaptic structures

17
Q

What are the properties of LTP?

A
  1. Co-operativity–multiple axons acting simultaneously produce more LTP than a single axon
  2. Associativity–pairing a weak input with a strong one can strengthen the response to the weak input
  3. Facilitation–neurons that work together have stronger synapses.
  4. It occurs in the hippocampus and cerebral cortex.
18
Q

What are physical changes to the synapse involved in LTP?

A
  1. Forming collaterals
  2. Increased NT release
  3. More postsynaptic receptors
  4. Thicker/smaller neck of dendritic spine
  5. Perforated synapse formation
  6. ^ transport
  7. ^ size/area of terminal
  8. ^ number of synaptic vesicles
  9. ^ density of contact zones
  10. ^ size/number dendritic spines
  11. ^ protein transport for spine construction
  12. Lowered synaptic cleft size
19
Q

Loss of CA1 neurons results in:

A

Anterograde amnesia

20
Q

Damage to the hippocampal formation causes:

A

~10 years of retrograde amnesia

If medial temporal lobe also damaged, ~30 years

21
Q

Pyramidal neurons project:

A

From forebrain to hindbrain

22
Q

Metabolic disturbance of the CA1 region can result in

A

Excess glutamate release, which causes a buildup of calcium, leading to cell death (anterograde amnesia)

23
Q

Damage to perirhinal and parahippocampal cortices can result in:

A

Anterograde amnesia

24
Q

Pyramidal neurons are mainly in the:

A

Hippocampus

25
Q

Removing PKC takes away

A

Place cell field stability

26
Q

Knocking out NMDAR1 receptor disrupts

A

Spatial memory

27
Q

Anticholinergics do what to learning:

A

Impair it

28
Q

Early in Alzheimer’s disease, neurons that secrete ___ are lost

A

ACh

29
Q

How are ACh neurons linked to memory?

A

Release of ACh makes cortical neurons more sensitive to tones that have been previously paired with arousing stimuli.

30
Q

Where do ACh neurons (in learning) project to and from?

A

From the nucleus basalis to the neocortex

From the medial septum to the hippocampus

31
Q

Damage to the lateral interpositus nucleus of the cerebellum causes:

A

Complete loss of the conditioning response.

32
Q

Suppression of the red nucleus causes:

A

A lack of response, but not a lack of actual learning

33
Q

Can brain damage impair LTM and STM independently?

A

Yes

34
Q

Why does emotional experience enhance memory storage?

A

Emotional experiences activate sympathetic NS, which releases epinephrine from medulla.

Epinephrine stimulates vagus nerve and raises blood glucose levels. This increases production/release of ACh and NE.

35
Q

How does NE improve memory storage?

A

NE increases stimulus salience by boosting signal:noise ratio.

36
Q

The bGH mice were ____ and learned ____.

A

Bigger and learned slower.

37
Q

The GHA mice were ____ and learned _____.

A

Smaller and learned faster.